Pulmonary fibrosis (PF) is a potentially fatal disorder associate with lung diseases that affect the lower respiratory tract. It is characterized by a major inflammatory response which etiology is not known. Inflammatory and immune cells alter the normal architecture of the lung by a repair mechanism that increases the proliferation of fibroblasts and deposition of collagen leading to fibrosis. Some of the human lung diseases that manifest fibrosis, as well as animal models that use administration of the antineoplastic drug Bleomycin (BLM) to induce this disorder, are associated with a major infiltration of lymphocytes, predominantly T-lymphocytes. The main goal of our project is to investigate the role that T-lymphocytes play in the induction and/or regulation of this fibrotic process using the BLM/mouse model. We have studied the population of T-lymphocytes that are present in the lung during PF using flow cytometry to determine the expression of CD4, CD8 and the a/B or y/8 T-cell receptor (TCR). The usage of different TCR chains was studied by PCR using V specific primers. We are currently studying how the susceptibility to PF is affected in TCR Transgenic mice that are restricted in the repertoire of TCR they can express. The result of these experiments will be discussed.